Oligodendroglial cell death induced by oxygen radicals and its protection by catalase

  title={Oligodendroglial cell death induced by oxygen radicals and its protection by catalase},
  author={Y. S. Kim and Seung U. Kim},
  journal={Journal of Neuroscience Research},
The cytotoxic effects of oxygen radicals have been studied in enriched population of mature bovine oligodendrocytes in culture. Oxygen radicals were generated enzymatically by glucose and glucose oxidase, and hypoxanthine and xanthine oxidase combinations. Cytotoxicity was assessed by trypan blue exclusion and percentage lactate dehydrogenase release into the culture media. Incubation of bovine oligodendrocytes with these oxygen radical‐generating systems for 4 hr resulted in significant cell… 
Mode of cell injury and death after hydrogen peroxide exposure in cultured oligodendroglia cells.
Oxidative stress has been implicated as a causal factor in a wide variety of neurodegenerative diseases. To investigate the direct consequences of oxidative damage on myelin-forming cells, we have
Glutathione Peroxidase-Catalase Cooperativity Is Required for Resistance to Hydrogen Peroxide by Mature Rat Oligodendrocytes
Evidence is provided for a key role for GPx-catalase cooperativity in the resistance of mature OLs to H2O2-induced cell death.
Oxygen radical‐induced neurotoxicity in spinal cord neuron cultures
Results indicate that both oxygen radicals and excitotoxic amino acids were involved in the oxidant‐ititiated neurotoxicity of spinal cord neurons.
Peroxide‐scavenging deficit underlies oligodendrocyte susceptibility to oxidative stress
The objectives of the present study were to compare several parameters important in the ability to scavenge peroxides between astrocytes and oligodendroglia.
Delayed oligodendrocyte degeneration induced by brief exposure to hydrogen peroxide
Vulnerable oligodendrocytes are exposed to oxidative stress that induces rapid degeneration and ultimately leads to delayed cell death, which is highly relevant to oligodendedrocyte damage and depletion following ischemic, traumatic, or inflammatory insults to the central nervous system (CNS).
Peroxynitrite‐induced oligodendrocyte toxicity is not dependent on poly(ADP‐ribose) polymerase activation
The results show that peroxynitrite exerts cytotoxic effects on oligodendrocytes in vitro independently of PARP activation, and the effects of the PARP inhibitors 3‐aminobenzamide (3AB) and 5‐iodo‐6‐amino‐1,2‐benzopyrone (INH2BP) on mitochondrial function and cell death in oligod endocrine cells.
Oligodendroglial cells in culture effectively dispose of exogenous hydrogen peroxide: comparison with cultured neurones, astroglial and microglial cells
It is demonstrated that oligodendroglial cells in culture have a prominent machinery for the disposal of hydrogen peroxide, which is likely to support the protection of these cells in brain against peroxides when produced by these or by surrounding brain cells.
Effects of Nerve Growth Factor on Glutathione Peroxidase and Catalase in PC 12 Cells
NGF can provide cytoprotection to PC12 cells by inducing the free radical scavenging enzymes catalase and GSH Px and reducing the number of reactive oxygen species in the cell line.


Liposome-mediated augmentation of catalase in alveolar type II cells protects against H2O2 injury.
An in vitro model of alveolar epithelial oxidant injury was developed based on exposure of cultured rat type II pneumocytes to superoxide and hydrogen peroxide enzymatically generated in the culture medium and partial and complete protection against oxidation injury was achieved by pretreatment of cells with catalase liposomes.
Suppression of experimental autoimmune neuritis by the oxygen radical scavengers superoxide dismutase and catalase
These findings underscore the importance of macrophages in EAN and provide evidence that, in this model, macrophagederived reactive oxygen intermediates contribute to damage of the myelin sheath.
Role of hydrogen peroxide in neutrophil-mediated destruction of cultured endothelial cells.
It is proposed that human neutrophils can destroy cultured human endothelial cells by generating cytotoxic quantities of hydrogen peroxide.
Effects of antioxidants on oxidant-induced sister chromatid exchange formation.
The findings suggest that the hydroxyl radical has an important role in the production of phagocyte-induced cytogenetic injury, membrane-derived intermediates may be involved, depletion of intracellular glutathione renders cells more susceptible to this injury, and supplementation of target cells with antioxidants can protect them from oxygen radical-generated chromosomal injury.
Mechanisms of the killing of cultured hepatocytes by hydrogen peroxide.
Oxygen radicals mediate endothelial cell damage by complement-stimulated granulocytes. An in vitro model of immune vascular damage.
An in vitro model of granulocyte-induced cytotoxicity was constructed utilizing 51Cr-labeled human umbilical vein endothelial cell cultures, suggesting that close approximation of the granulocytes and endothelial cells is necessary for maximal cell injury.
Appearance of Superoxide Anion Radical in Cerebral Extracellular Space during Increased Prostaglandin Synthesis in Cats
Results show that most of the nitroblue terrazolium reduction was accounted for by superoxide anion radical generated in the course of arachidonate metabolism via the cyclooxygenase pathway, and the most likely explanation for these findings is that increased metabolism of exogenous or endogenous archidonate via cyclo oxygengenase results in the appearance of superoxideAnion radical in cerebral extracellular space.
Oxidant injury of cells.
Inhibitors of poly-ADP-ribose polymerase prevented cell lysis, but not DNA damage, and was proposed to be a suicide mechanism for cells with irreversibly damaged DNA.